Karyotypic changes through dysploidy persist longer over evolutionary time than polyploid changes

Marcial Escudero, Santiago Martín-Bravo, Itay Mayrose, Mario Fernández-Mazuecos, Omar Fiz-Palacios, Andrew L. Hipp, Manuel Pimentel, Pedro Jiménez-Mejías, Virginia Valcárcel, Pablo Vargas, Modesto Luceño

Research output: Contribution to journalArticlepeer-review

Abstract

Chromosome evolution has been demonstrated to have profound effects on diversification rates and speciation in angiosperms. While polyploidy has predated some major radiations in plants, it has also been related to decreased diversification rates. There has been comparatively little attention to the evolutionary role of gains and losses of single chromosomes, which may or not entail changes in the DNA content (then called aneuploidy or dysploidy, respectively). In this study we investigate the role of chromosome number transitions and of possible associated genome size changes in angiosperm evolution. We model the tempo and mode of chromosome number evolution and its possible correlation with patterns of cladogenesis in 15 angiosperm clades. Inferred polyploid transitions are distributed more frequently towards recent times than single chromosome gains and losses. This is likely because the latter events do not entail changes in DNA content and are probably due to fission or fusion events (dysploidy), as revealed by an analysis of the relationship between genome size and chromosome number. Our results support the general pattern that recently originated polyploids fail to persist, and suggest that dysploidy may have comparatively longer-term persistence than polyploidy. Changes in chromosome number associated with dysploidy were typically observed across the phylogenies based on a chi-square analysis, consistent with these changes being neutral with respect to diversification.

Original languageEnglish
Article numbere85266
JournalPLoS ONE
Volume9
Issue number1
DOIs
StatePublished - 9 Jan 2014

Funding

FundersFunder number
Seventh Framework Programme301119

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